Mental disorders in brain injuries
The course of traumatic disease is divided into several stages, each with its own psychopathological profile.
Acute period Loss of consciousness occurs immediately after the injury. If the coma lasts more than 30 days, acceptable mental recovery is practically impossible. Emergence from prolonged coma occurs strictly in stages: eye movements return first, then emotional reactions to loved ones, and only lastly does spontaneous speech recover. After waking up, episodes of global amnesty, short-term hypomania, or acute psychoses (delirium, oneiroid state) are frequently observed. Pronounced memory impairments follow the pattern of Korsakoff's amnestic syndrome, which may partially regress over time.
Convalescence period and long-term sequelae During recovery, asthenia (fatigue, load intolerance) and somatovegetative disorders come to the forefront. If the injury was mild, the patient recovers, but increased vulnerability and alcohol intolerance may persist. With a severe organic deficit, chronic conditions form:
- Post-traumatic cerebropathy: neurotic level of disorders. The patient suffers from insomnia and irritability. The condition improves after rest, but any new stress leads to severe decompensation.
- Post-traumatic encephalopathy: a persistent deficit with Korsakoff's syndrome, intellectual decline, and epileptic seizures. Personality changes: pettyness, stubborness, viscosity (torpidity), and vindictiveness increase. With massive damage (e.g., contusion of the frontal lobes), disinhibition, inadequacy, fits of rage, and gross stereotypies are observed.
Management of disorders in traumatic brain injuries
The basis of therapy in the acute period is strict bed rest, dehydration (acetazolamide, furosemide), and nootropic support.
To relieve psychiatric complications, the following are used:
- Antipsychotics: for psychotic agitation (risperidone, quetiapine). Prescribed in low doses along with correctors. It is important to remember that excessive sedation severely impairs the patient's memory.
- Antidepressants: for the development of persistent post-traumatic depression. It is strictly forbidden to use drugs with pronounced anticholinergic activity — they provoke the development of delirium.
- Normotimics (mood stabilizers): valproic acid preparations or carbamazepine. Carbamazepine is especially valuable because it not only blocks epileptiform paroxysms but also smooths out psychopath-like manifestations, reducing irritability and aggressiveness.
Mental disorders due to intoxication
The symptoms of poisoning by various poisons have colossal similarity, fitting within the framework of exogenous reactions. Acute severe poisonings switch off consciousness up to coma. Less dangerous intoxications debut with dizziness, nausea, and euphoria, which may be followed by psychoses. The most frequent intoxication psychosis is delirium (especially in poisoning with anticholinergics).
Chronic intoxications and Wernicke's syndromes With prolonged exposure to poisons, asthenia, depression, and Korsakoff's syndrome develop. A special place is occupied by transition syndromes (described by C. Wernicke). They lie on the border between acute psychosis and irreversible dementia. Their main feature is a tendency to regress. That is, unlike persistent psychoorganic syndrome, transitional states can show significant improvement after the cessation of intoxication.
Drug-induced psychoses Poisoning can be iatrogenic due to individual intolerance or overdose:
- Antiparkinsonian and anticholinergic agents frequently cause delirium.
- Glucocorticoids and estrogens in high doses provoke euphoria, severe insomnia, and hallucinatory-paranoid psychoses, externally very resembling schizophrenia attacks.
Briefly: answers to topical questions
What types of amnesia are distinguished in traumatic brain injuries depending on the period of memory loss?
In traumatic brain injuries, depending on the period of memory loss, two main types of amnesia are distinguished.
- Anterograde amnesia — the inability to remember events that occurred after the injury (complete inability to retain new information in memory).
- Retrograde amnesia — the inability to recall events that occurred before the injury (erasing a small segment of time from memory immediately preceding the onset of the disease).
Which drugs are used as correctors for extrapyramidal disorders when prescribing antipsychotics?
As correctors for extrapyramidal disorders caused by antipsychotic intake, the following drug groups are used:
- Anticholinergics — trihexyphenidyl (cyclodol), biperiden (akineton), diphenhydramine (dimedrol).
- Adamantane derivatives — amantadine (midantan, PK-Merz).
- Beta-blockers — used for akathisia and tardive dyskinesia.
- Benzodiazepine tranquilizers — used for acute spasms and tardive dyskinesia.
- Metoclopramide can also be used for acute spasms.
Levodopa is not prescribed because it can provoke an exacerbation of psychosis.
What periods are officially distinguished in the clinical course of traumatic brain disease?
In the clinical course of traumatic brain disease (traumatic brain injury), three periods are distinguished.
- Acute period — occurs immediately after the injury, manifested by loss or clouding of consciousness, transient amnesia.
- Convalescence period — lasts several months, accompanied by gradual improvement, asthenia, somatovegetative disorders, and depression.
- Period of long-term sequelae (chronic course) — develops in some patients, manifested by post-traumatic cerebropathia, encephalopathy, personality changes, and persistent memory disorders.
To remember the sequence of functional recovery upon emerging from a long coma, use the rule «GIR»: G — Gaze (tracking), I — Interaction (emotions toward loved ones), R — Speech (own words).
Class and exam questions
Why should antidepressants with anticholinergic action not be used in the treatment of depression in patients with TBI?
In patients with organic brain damage, anticholinergics carry a high risk of provoking confusion and developing severe delirium.
What are Wernicke's transition syndromes?
These are transitional states between acute exogenous psychosis and persistent organic brain deficit in poisonings. Unlike formed encephalopathy, they tend to regress and improve.
What else to study on this topic
- Clinical analysis of the behavior and symptoms of a patient with severe frontal lobe damage.
- Differential diagnosis of intoxication (steroid) psychoses and endogenous schizophrenia.
- Pathogenesis of cerebrospinal fluid dynamics disorders and its role in the development of paroxysmal hallucinatory psychoses in the long-term period.
- Specific hallucinoses in poisoning with psychostimulants (cocaine) and heavy metal salts.
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Other topics in "Chapter 19. Organic, Exogenous, and Somatogenic Mental Disorders"
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